Morphology and Biology of Viruses Flashcards

Question

Describe the clinical manifestations of parovirus

Answer 1

"slapped-cheek" rash, red rash on trunk and limbs. May have a low-grade fever, malaise a few days before the rash breaks out. Rash may itch. Resolves in 7-10 days Gloves and socks syndrome Arthropathy Transient aplastic crisis Chronic red cell aplasia Neutropenia, thrombocytopenia and pancytopenia

Answer 2

Respiratory route mother to the foetus transmission - this is more of a concern in the first trimester and if the mother does not have IgG antibodies against the virus No specific drug to treat Parvovirus B19 infection.

Answer 3

Airborne virus producing feverish illness Causes serious illness in immunocompromised Orthomixoviridae (family) lipid envelope derived from host cell membrane.

Answer 4

These are embedded in the lipid bilayer of the viral envelope. Matrix protein 2, M2= ion channel protein The ribonucleoprotein complex comprises viral RNA segments associated with the viral proteins. The matrix (M1) protein is associated with both ribonucleoprotein and the envelope.

Answer 5

Type A - Most serious, affects mammals and birds Genetic cross-over between strains can lead to pandemic Subtyped according to its surface Ags- (HA) and (NA) Type B: affects humans, minor outbreaks C: affects humans, endemic, similar to common cold

Answer 6

Uses haemagglutinin to attach to sialic acid, enters by endocytosis Virus envelope fuses w endosome, triggering uncoating Viral nucleocapsid released into cytoplasm Copies of viral RNA and mRNA made, mRNA translated in cytoplasm Early viral proteins required for replication/transcription are transported back to the nucleus. Late in infection cycle, M1 and NS2 proteins facilitate nuclear export of newly made viral ribo nuclear proteins. RNA segments assembled within nucleocapsid and bud at plasma membrane

Answer 7

Surface Ags of Influenza A mutate rapidly bc: Viral RNA polymerase involved in replication has low selectivity and no proof reading mechanism Therefore mutants are generated and spread rapidly. Two patterns of mutation: antigenic drift and antigenic shift

Answer 8

Continual viral mutation Mutations are often minor with no effect on function Changes accumulate to create new “drifted strains” Drifted strains produce illness Some strains co-exist Occurs in around 2 to 8 years

Answer 9

Type A only Genetic reassortment: mixing genetic material between strains, when they infect the same host Creates novel strains ppl dont have immunity to. Rapid spread - pandemic Mixed strains from diff species= mas virulent/fuera control

Answer 10

Global Influenza Network estimate the strain of virus before the following season and recommend vaccines Limitations: errors in the estimate manufacturing difficulties time constraints, lack of resources antigenic drift continues (vaccine mismatch)

Answer 11

HIV Gp120 protein binds to CD4. CCR5 T co receptor binds Gp120, enabling HIV to enter the T helper cell. Reverse transcriptase copies viral RNA-> double stranded proviral DNA, which then undergoes ps. Virus envelope proteins are also translated, transported in the G.app.Virus envelope proteins incorporate onto cell membrane. Virus particle buds from the host cell, becoming wrapped in the cell membrane, producing a new viral envelope.

Answer 12

Replication at the site of entry Remain at the site of entry Examples: Influenza, Rhino virus Replicate at site of entry then spread, eg VZ virus

Answer 13

Infection with a 2nd organism, eg Candida albicans (thrush) if patient given antibiotics that have removed the protective flora 2* infections can also happen following an infection eg HIV that compromises immunity Bacterial pneumonia can also happen after viral respiratory tract infections in a healthy individual.

Answer 14

Faecal oral route: Norovirus, Rotavirus Blood: HIV, Hepatitis B and C Body fluids: Epstein Barr virus Resp tract: Influenza, Rhinovirus, VZ virus Skin cuts: Papilloma, Mol.contagiousum (Poxvirus) Sexual: Papilloma, Herpes simplex virus, HIV Animal/insect bites: Lassa fever

Answer 15

Acute: Rabies, Rhinovirus, Influenza, Rotavirus Chronic: Hep B and C, but in some cases infection can be cleared

Answer 16

Vertical transmission: Foetus unable to mount immune response. Mode of entry also via placenta eg rubella can be transmitted--> congenital rubella Parvovirus infection in pregnancy – most of us have Abs to Parvovirus B19. Infection can show slapped cheek appearance – during early stages of pregnancy risk of hydrops fetalis.

Answer 17

Latency: After primary infection, enter sites eg dorsal root ganglia, remain latent. Don't replicate fully, evade detection. Replicate in privileged sites: HIV. Cytomegalovirus: downregs MHC I, hinders Ag presentation Release decoy particles: diverts response, eg Hep B

Answer 18

Non-enveloped Circular double stranded DNA More than 100 HPV types identified High risk: HPV 16, 18, 31, 45 Linked to development of cervical carcinoma and other malignancies

Answer 19

Virus infects epithelial cells, which have dif layers and differentiate As cells leave basal layer and move up they stop dividing- If cell is not replicative virus may struggle to replicate So, virus infects basal layers, migrates to cell nucleus Genome established, replication can occur

Answer 20

HPV encodes early genes(E2,6,7) + late genes(L1,2) E6 interferes w P53 tumour suppressor protein E7 interferes w retinoblastoma tumour suppressor E2 inhibits E6 and E7 (cancer causing) expression As HPV integrates into host genome, E2 viral gene splits E2 ya no functions, E6 and 7 expression not inhibited Uncontrolled E6/E7 oncoproteins=epithelial cells cannot leave the cell cycle E6 also activates the telomerase gene Cancer cells make telomerase which keeps telomere intact. Cells do not age and continue to divide

Answer 21

Flaviviridae family Enveloped, single strand +sense RNA Small – 50nm Transmitted by mosquitoes Number of infants born with microcephaly high in areas where Zika virus was first reported- first trimester at greatest risk.